RNF20 deletion causes inflammation in model of sepsis through the NLRP3 activation

Qi, Anlong; Liu, Yan-Cun; Zhai, Jianhua; Wang, Yongtao; Li, Wang; Wang, Tong; Chai, Yanfen

doi:10.1080/08923973.2023.2170241

Cited by 1 publication

(1 citation statement)

References 31 publications

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“…Studies have confirmed the essential role of RNF20 in several physiological processes including cell differentiation, spermatogenesis, and adipose tissue development (29,32,34). Furthermore, RNF20 deficiency in association with some pathological processes such oncogenesis and inflammation has also been extensively explored (35)(36)(37). Although the fundamental role of RNF20 has been recognized under both physiological and pathological conditions, the connection between RNF20 and its downstream target H2Bub1 in the ID context has never been systematically explored.…”

Section: Introductionmentioning

confidence: 99%

Iron deficiency–induced ferritinophagy impairs skeletal muscle regeneration through RNF20-mediated H2Bub1 modification

Che,

Li,

Wang

et al. 2023

Sci. Adv.

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Iron deficiency (ID) is a widespread condition concomitant with disease and results in systemic dysfunction of target tissues including skeletal muscle. Activated by ID, ferritinophagy is a recently found type of selective autophagy, which plays an important role in various physiological and pathological conditions. In this study, we demonstrated that ID-mediated ferritinophagy impeded myogenic differentiation. Mechanistically, ferritinophagy induced RNF20 degradation through the autophagy-lysosomal pathway and then negatively regulated histone H2B monoubiquitination at lysine-120 in the promoters of the myogenic markers MyoD and MyoG , which inhibited myogenic differentiation and regeneration. Conditional knockout of NCOA4 in satellite cells, overexpression of RNF20 or treatment with 3-methyladenine restored skeletal muscle regenerative potential under ID conditions. In patients with ID, RNF20 and H2Bub1 protein expression is downregulated in skeletal muscle. In conclusion, our study indicated that the ferritinophagy-RNF20-H2Bub1 axis is a pathological molecular mechanism underlying ID-induced skeletal muscle impairment, suggesting potential therapeutic prospects.

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